98 Part IV / Mechanical Complications
diastolic blood pressure above 75 mm Hg may reflect the association between
hypertension and VSR.
On the other hand, the negative correlations between VSR incidence and enrollment
systolic blood pressure (≤130 mm Hg) and diastolic blood pressure (≤75 mm Hg) may
relate to the occurrence of hemodynamic compromise associated with extensive MI or
right ventricular infarction, both of which are established risk factors for VSR (9). The
presence of right bundle-branch block with or without fascicular block, advanced atrio-
ventricular block, or atrial fibrillation may occur more frequently in patients with VSR
than in patients with free wall rupture (19,21,22).
Pathophysiology
After an MI, VSR generally develops at the margins of the necrotic and non-necrotic
myocardium. The size of VSR ranges from a few millimeters to several centimeters.
The septal tissue adjacent to the defect is often thin and necrotic, whereas the septum
may be fibrotic in patients who die several weeks after the development of the VSR.
Some patients develop a septal aneurysm adjacent to the rupture site. In addition, the
rupture of other cardiac structures such as papillary muscles and the free wall of the left
and/or right ventricles may occur concomitantly (10,19,23,24).
Morphologically, VSR can be categorized into simple and complex forms. Simple
VSR is a discrete hole with a direct through-and-through communication across the
septum. The ventricular openings are located at the same level on both sides of the sep-
tum. Complex VSR is characterized by extensive hemorrhage around irregular serpigi-
nous tracts extending in different directions within extensive necrotic tissue (10,18).
Complex ruptures are more likely to affect associated structures such as the right ven-
tricle (10). VSRs in anterior acute MI tend to be apical and simple, whereas in inferior
acute MI, they involve the inferobasal septum and are usually complex (6,10,18). Most
patients with VSR complicating both anterior and inferior MI have evidence of right
ventricular infarction (16).
Ventricular septal rupture is complicated by left-to-right shunting, which results in
right ventricular volume overload, increased pulmonary blood flow, as well as volume
overload of the left atrium and left ventricle. As the left ventricular systolic function
deteriorates and forward flow declines, compensatory vasoconstriction triggers an
increase in systemic vascular resistance and in the magnitude of left-to-right shunt. The
severity of the left-to-right shunt is determined by the size of the VSR, relative changes
in the pulmonary and systemic vascular resistances and pressure, and left ventricular
performance (14).
Another pathophysiologic characteristic of VSR is that the condition may coexist
with mitral regurgitation (MR). Ten to 20% of patients with VSR also have severe MR
(25,26), which may be the result of concomitant papillary muscle ischemia or infarc-
tion, dilatation of the mitral annulus, or deformation of the left ventricle with alteration
of the geometry of the mitral apparatus (13,22).
Angiographic Findings
In studies using angiographic data, investigators have consistently demonstrated that
patients with VSR are more likely to have total occlusion of the infarct-related artery
(6,9,13,27). In patients who underwent angiography in the GUSTO-I study, total occlu-
sion of the infarct-related artery was documented in 57% of patients with VSR and
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